Upon physical examination Tommy turns out to have a "Soft, low pitched apical pan-systolic murmur is heard radiating to the axilla."
What pathological change in the heart is causing this murmur?
A mitral/tricuspid valve incompetence.
If Tommy's heart is failing to effectively pump blood around the body, why doesn't the heart undergo hyperplasia and increase the number of cardiomyoctes? Why hypertrophy?
If there is mitotic divisions happening the intrinsic conduction system of the heart finds it too difficult to compensate.
In Tommy's case with his acute heart failure why wouldn't you give a him beta-1 agonist?
WOW HAP QUESTION WORTH 600 POINTS
How much more likely are indigenous Australians like Tommy to die from RHD? Why are they more likely to suffer from it's long term consequences?
20x more likely
WORST IN THE WORLD
SOCIAL DETERMINANTS
A good drug only targets pathogens without damaging human cells. What is this desirable property called?
Selective toxicity
Tommy presents with the following CXR: Patient (indicates pulmonary oedema and cardiomegaly and Kerley B lines)
What is the difference between effusion and oedema? List 4 places you could find effusion.
While oedema is fluid in the subcutaneous tissues, effusion is fluid in ‘potential spaces’ as well as subcutaneous tissues.
Potential spaces are:
The extent of Tommy's heart failure can be measured by a specific blood test. What is it?
B-type natriuretic peptide protein secreted by the ventricles during excessive stretching
Crescendo-decrescendo murmur that occurs during systole.
What bacteria causes strep throat and the severe problems related to rheumatic fever including anemia.
Group A hemolytic streptococci
List the 3 drug classes that inhibit protein synthesis and an example for each.
TAM (like TIMTAM YUM)
Tetracyclines - doxycycline
Aminoglycosides - gentamicin
Macrolides - erythromycin
List the 5 types of shock and briefly describe them.
While Tommy has no history of smoking or alcohol consumption, what is the most common idiopathic toxic cause of dilated cardiomyopathy?
Alcohol. 1/3 of dilated cases.
What causes the processes in the compensated heart to eventually fail?
High filling volumes (>150mls) leads to high resistance in ventricules during passive ventricular filling. Any further EDV leads to an loss of the increased contractile strength of cardiomyocytes, as they are overstretched.
Tommy has had rhuematic fever as a child. What is the JONES criteria for rheumatic fever?
What class of macromolecule synthesis are sulfonamides a part of? What does it inhibit?
Class II - Exploit some difference between human & bug – eg. Vitamin, AA synthesis
Folate synthesis
"Tommy has short of breath while at rest, sitting upright, using accessory muscles of respiration, centrally cyanosed, coughing up pink frothy sputum."
What is happening currently in Tommy's lungs for him to have SOB?
Currently there is back flow of blood from the left ventricle into the pulmonary circuit during systole. This effectively increases the hydro static pressure in the lungs' vasculature and results in fluid deposits into the interstitial fluid - oedema. This oedema reduces the efficiency of gas exchange in the alveoli and leads to SOB.
What is hypertrophic obstructive cardiomyopathy? (HOCM) How is it different to left ventricular hypertrophy?
Hypertrophic cardiomyopathy is generally caused by genetics and is related to an asymmetrical septal width. This obstruction of blood flow can lead to LVH.
Left ventricular hypertrophy is caused by a plethora of reasons and is characterised by a free left ventricular wall thickness >1.5CM.
What long term processes does the body use to compensate heart failure?
Tommy suffers from "atrial fibrillation and acute cardiac failure, secondary to rheumatic heart disease (RHD)." What macroscopic and microscopic changes would you expect to see on his mitral valve?
Macroscopic
Vegetations --> fibrinoid necrosis
Microscopic
Aschoff body --> fibrinoid necrosis regions with immune cells
Anitschkow cells --> 'caterpillar cells' with oval nuclei
How do beta-lactams work? List two examples.
BONUS: +400 points How is it different to vancomycin?
Enzyme called transpeptidase (penicillin binding protein) is needed
Binds to transpeptidase enzyme preventing bacterial wall synthesis
Amoxycillin & cefalexin
Vancomycin binds to the peptide chains and prevents them from interacting properly with the cell wall cross-linking enzyme.
Tommy's "The trans-oesophageal ECHO reveals moderate mitral regurgitation. His left ventricular function is borderline normal with no atrial dilatation."
What pathological (microscopic) changes would you expect to develop in Tommy's lungs if his left ventricle continued to fail?
Congestion in the lungs from left ventricular failure.
Engorged (dilated) alveolar capillaries (below)
Then ruptures/hemorrhages into alveoli spaces
Thickened septa with fibrosis
Siderophages – heart failure cells
Macrophages with hemosiderin
Hemosiderin is an iron carrying protein in the blood
What is restrictive cardiomyopathy?
Restrictive filling--> poor EDV and preload either or both ventricles
Normal/near normal ventricular function --> systolic function and wall thickness.
Heart walls are rigid but not thickened
If left untreated Tommy's acute heart failure could results in a myocardial infarction. What are the 4 steps in the recovery of the heart following an MI?
List the 3 layers of heart valves and what they compose of.
Explain the MOA for quinolones and an example drug. What enzymes are inhibited?